Altered LOC differentials and presentations Flashcards
Differentials
-SAH
-stroke/ TIA
-syncope
-hypoglycaemia
-hyperglycaemia
-intoxication
-opiate OD
-addisons
-CO poisoning
-sepsis
-epileptic seizure
-AKI
-meningitis
SAH path
-undiagnosed ‘berry’ aneurysm whic ruptures
-causes bleeding between pia mater and arachnoid mater (in subarachnoid space)
-blood then build up around the brain increasing intercranial pressure
-leads to early brain injury or transient global cerebral ischaemia
SAH presentations
-sudden headache- ‘thunderclap’
-stiff neck
-nausea/ vomiting
-photophobia
-blurred/ double vision
-focal neurological deficit
-confusion
-reduced LOC
-single fixed dilated pupil (bad)
-bilateral fixed dilated pupils (worse)
Stroke path
-clinical syndrome characterised by SUDDEN onset of rapidly developing focal or global neurological disturbance which lasts more than 24 hours of leads to death
Haemorrhagic stroke (15%)
-caused by blood vessel rupture, bleeding in the brain
Ischaemic stroke (85%)
-blockage of one of the cerebral blood vessels
Stroke presentation
-confusion, reduced LOC
-headache- sudden and severe
-weakness- face, limbs
-sensory loss- paraesthesia or numbness
-speech problems
-visual problems
-dizziness/ vertigo
-nausea/ vomiting
-loss of coordination
-specific cranial nerve deficits
Syncope path
-reduction in systemic BP, causing decrease in global cerebral flow and reduced LOC
-as we age we become more susceptible to small falls in BP, increased incidence of syncope
-many causes with unique pathophysiological cause
Pre syncope presentations
-light headed
-sweating
-nausea
-visual disturbance
Signs of a simple faint and in absence of red flags and with full recovery, discharge on scene
Hypoglycaemia pathophysiology
-blood glucose drops below 4 mmol/L
-triggers cascade of physiological responses aimed to restore BM levels
Caused by
-increased insulin, decreased glucose production, increased glucose utilization, reduced glucose intake
-leads to adrenergic symptoms (activation SNS) and neuroglycopenic symptoms inadequate glucose to brain)
Hypoglycaemia presentations
Adrenergic (autonomic) symptoms
-diaphoresis
-tremors/ shaky
-palpitations
-anxiety
-hunger
-pallor
Neuroglycopenic symptoms
-dizzy/ light headed
-confusion
-slurred speech
-burred vision
-weakness/ fatigue
-seizures in severe cases
-LOC
Other
-nausea, headache
Hyperglycaemia path
-elevated BM (higher than 7.8)
-imbalance between glucose production and glucose utilization
1. impaired glucose utilization- type 1 (destroy pancreatic b cells, less insulin produced), type 2 (insulin resistance)
2. increased hepatic glucose production- insulin deficiency/ resistance causes liver to continue gluconeogenesis and glycogenolysis (glucagon to glucose)
Hyperglycaemia presentations
-polyuria
-polydipsia (thirsty)
-polyphagia (hunger)
-fatigue
-blurred vision
-headaches
Severe
-dehydration
-altered mental status
-DKA
Opiate OD path
-excessive opioids bind to receptors in CNS leading to resp and CNS depression
-Respiratory depression by suppressing medullary respiratory centres reducing brains response to CO2
-CNS depression- suppression of reticular activating system leading to reduced LOC, coma
Opiate OD presentations
-resp depression- slow/ stop breathing
-CNS depression- unresponsiveness/ coma
-miosis- pinpoint pupils
-slurred speech
-confusion
-hypotension
-nausea and vomiting
Addisons path
-adrenal glands don’t produce enough cortisol and aldosterone
-destruction of adrenal cortex
-hormonal imbalances
Addisons presentations
-chronic fatigue
-weight loss
-hyperpigmentation
-hypotension/ dizzy
-salt craving
-hypoglycaemia
Adrenal crisis
-severe hypotension -> shock
-severe hypoglycaemia
-confusion
CO poisoning path
-CO binds to haemoglobin in erythrocytes
-higher affinity than O2 so less O2 able to bind
-leads to hypoxia, cell damage
CO poisoning presentations
-headache
-dizzy/ confusion
-nausea and vomiting
-fatigue
-SOB
Severe
-LOC
-seizure
-cardiac arrhythmias
-metabolic acidosis
Sepsis path
-pathogens release pathogen associated molecular patterns
-these are recognised by pattern recognition receptors
-this triggers massive inflammatory cytokine release
-this leads to increased vascular permeability, vasodilation, activation of coagulating cascade
Sepsis presentations
-fever or hypothermia
-tachycardia
-tachypnoea
-altered mental status
Severe
-hypotension
-oliguria
-lactic acidosis
Seizure path
-sudden uncontrolled electrical disturbance in brain caused by excessive neuronal firing
-focal seizures- starts in one part of brain
-generalized- both hemispheres from onset
Due to
-increased synaptic excitation, eg. glutamate -> overactivation of NMDA receptors -> excessive Ca2+ -> increased neuronal firing
-failure of inhibition -> reduced GABA activity -> less inhibition -> uncontrolled neuron firing
-ion channel dysfunction
Seizure presentations
Focal
Simple- no LOC, jerking in one limb
Complex- impaired awareness, automatisms
Generalized
-tonic clonic- stiffening (tonic), rhythmic jerking (clonic)
-absence- staring (common in children)
-myoclonic- sudden muscle jerks, no LOC
-atonic- loss of muscle tone
Meningitis presentations
-severe headache
-stiff neck
-dislike bright lights
-haemorrhagic, non blanching rash (only 40%, very late sign)
Kernig sign
-lie flat on floor
-knee flexed to 90 degrees
-hip flexed 90 degrees
-extension of knee is painful or limited in extension
Brudzinski sign
-lie on floor
-bring head forward
-reflex action causing hip and knee flexion
Meningitis pathophysiology
-bacteria or virus in body
-crosses BBB and enters CSF
-recognised by immune system tiggering massive inflammatory response (cytokine, prostaglandins)
-increases permeability BBB, increases ICP
-causes meninges to swell, compressing BV, reducing cerebral perfusion
-disrupts CSF drainage leading to hydrocephalus (build up of fluid on brain)
